| Objectives To observe therapeutical effect of new compound formulations of K-CoxB-JN to VMC mouse. Provide a theoretical basis and experimental evidence for the drugused in clinical.Methods1To establish the model of viral myocarditis in mice: Amplification ofCVB3in Hep-2cells. Determination of CVB350%tissue culture infective dose (TCID50).Seventy-eight male Balb/c mouse were selected and fed for one week.Then the mousewere divided into6groups randomly.Took one group as a control group, intraperitonealinjection of physiological saline0.2ml/only.The rest five groups were injected with CVB3the concentration of10-6,10-7,10-8,10-9,10-10,0.2ml/only.To establish the model of viralmyocarditis in mice.The general state of mouse and the number of deaths wererecorded.Mouse were sacrificed on fourteen days.Detected of serum myocardialenzymes, organ index.Did pathological examination of myocardial tissue.According tothe results of pre experiment determine viral inoculation in formal experiment.2Thetherapeutical effect of new compound formulations of K-CoxB-JN to CVB3myocarditisin mice:Two hundred and ten male Balb/c mouse were selected and fed for oneweek.Randomly took twenty mouse as a control group, intraperitoneal injection ofphysiological saline0.2ml/only.The rest mouse were injected with CVB30.2ml/only, toestablish the model of viral myocarditis in mice.Then randomly divided into5groups,new compound formulations of K-CoxB-JN with low, middle and high dose groups,ribavirin group, model group.The mouse were treated with new compound formulationsof K-CoxB-JN in low(0.2g/kg), middle(0.4g/kg), high dose (0.8g/kg),ribavirin(0.075g/kg)and pure water(0.2ml/10g) by gavage for14days.The generalstate of mouse and the number of deaths were recorded.In seventh day eight mouse wereselected randomly from each group, the fourteenth day the remaining mouse wereweighed.Blood samples were collected for the measurement of aspartateaminotransferase(AST), creatine kinase(CK)and lactate dehydrogenase (LDH).Then theheart, the spleen, the thymus were weighed to calculate organ index.Part of the heartswere taken in10%formaldehyde to fix, myocardial pathological changes were observedby HE staining and pathological score were recorded.Results1The results of model of viral myocarditis in mice:CVB3were passaged inHep-2cells, measured the TCID50was10-7.5/0.1ml.The general state, the number ofdeaths and the organ index were related to the concentration of the virus.Theconcentration of virus was10-7～10-10,mice mortality was less than50%.Theconcentration of virus was10-6,mice mortality was greater than50%.Serum myocardialenzyme activity were significantly increased.Myocardial tissue pathological changedsignificantly.Pathological integral was heavier than the other group P<0.05.Comparedwith the normal control group P<0.05.2The impact of new compound formulations of K-CoxB-JN on the general state and the number of deaths of VMC mice:Thegeneral condition of the normal group mouse were good.The model group mouse showedactivity and feeding was reduced, dull sparse fur and other symptoms.The treatmentgroups were better than the model group.The treatment groups were lower than the model group in the number of deaths.3The impact of new compound formulations of K-CoxB-JN on the viscera index of VMC mice:When the mouse were administered for7and14days, the normal group viscera index was lower than other groups P<0.05,thedifference was significant.The model group heart weight index was higher than othergroups P<0.05, the difference was significant.The thymus weight index and spleenweight index compared with the rest of the treatment groups P>0.05.Ribavirin group ofthe viscera index compared with the rest of the treatment groups P>0.05.Compared withthe14and7days, the viscera index in each group had a downward trend.4The impact ofnew compound formulations of K-CoxB-JN on the myocardial enzymes of VMC mice:When the mouse were administered for7and14days, the normal group AST、CK、LDH were lower than other groups P<0.05, the difference was significant.The modelgroup AST、CK、LDH were higher than other groups P<0.05.Ribavirin group ofAST、LDH compared with the low-dose group P<0.05.Compared with the middle doseand high dose groups P>0.05.Ribavirin group of CK compared with the rest of thetreatment groups P>0.05,the difference was not significant.Compared with the14and7days, AST、CK、LDH in each group had a downward trend.5The impact of newcompound formulations of K-CoxB-JN on the tissue pathological score of VMCmice:Observed under the light microscope, the normal group mice myocardial structuralintegrity,neatly arranged, no abnormal change.The model group mice myocardial disarray,myocardial cells in inflammatory cell infiltration and necrosis.The treatment groupscardiomyopathy compared with model group decrease significantly.When the mousewere administered for7and14days, the normal group tissue pathological score waslower than other groups P<0.05, the difference was significant.The model grouptissue pathological score was higher than other groups P<0.05.Ribavirin group of thetissue pathological score compared with the low-dose group P<0.05.Compared with themiddle dose and high dose groups P>0.05,the difference was not significant.Conclusions1Through intraperitoneal injection of the concentration of10-6CVB3could be successfully established the model of viral myocarditis in mice.2Newcompound formulations of K-CoxB-JN had therapeutic effect on viral myocarditis inmice.It could improve the quality of life and reduce the number of deaths of viralmyocarditis in mice.3New compound formulations of K-CoxB-JN could reduce the heartweight index of viral myocarditis in mice.4New compound formulations of K-CoxB-JNcould reduce the cardiac enzyme levels of viral myocarditis in mice.5New compoundformulations of K-CoxB-JN could reduce the myocardial pathological damage andtissue pathological score of viral myocarditis in mice. |
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